Background Patients with IBD are at higher risk for non-alcoholic fatty liver disease (NAFLD) comparing to general population. Complex pathogenesis of NAFLD in IBD may be related to disease-specific risk factors such as chronic inflammation, steroid exposure, drug induced hepatotoxicity, malnutrition and alteration of gut microbiota, which is emerging as a major factor in the pathogenesis of NAFLD. The goal of the study was to investigate factors associated with NADLF and advanced liver fibrosis (ALF) in patients with CD and UC. Methods This is a retrospective study on IBD patients without extraintestinal manifestations and known liver disease. NAFLD was defined as Hepatic Steatosis Index (HSI) ≥ 36, and ALF was defined as FIB-4 ≥ 2.67. Predictors of NAFLD development were analysed using Kaplan–Meier and Cox regression analyses. Results In this retrospective study, we have included 225 IBD patients; 72.4% (n = 163) patients with CD and 27.6% (n = 62) patients with UC (median age 41.2 yr, 53.7% males) which were observed for a median of 4.6 years. There were 63.1% (n = 142) patients with normal BMI, 27.6% (n = 62) overweight and 9.3% (n = 21) obese patients. Obese patients had the highest HIS score 43.9 ± 5.9, following with overweight 37.8 ± 5.7 and normal BMI 30 ± 4.3 kg/m2, p < 0.001. During the follow-up obese and overweight patients had higher risk of developing NAFLD comparing to patients with normal BMI (obese HR = 11.1 95% CI 4.3–28.3 and overweight HR = 5.55 95% CI 3.4–9.1, Logrank test p < 0.001) (Figure 1). Regarding FIB-4 score there, was no difference among different BMI categories (p = 0.192), and there was no difference in ALF development in the follow-up period (Logrank test p = 0.91). In Cox proportional-hazards regression significant predictors for NAFLD development were dyslipidaemia HR=2.11, 95% CI 1.2–3.7, overweight HR=6 95% CI 3.6–10, and obesity HR=13.4, 95% CI 7–35. Conclusion NAFLD is frequent comorbidity in patients with CD and UC, which can lead to development of advanced liver fibrosis. Our results show that patients with IBD have a high risk of NAFLD development, whereas the increased risk for ALF was not observed. Overweight and obese patients and those with dyslipidemia should be closer monitored due to significantly higher risk of NAFLD. This study points out the complexity disease-specific risk factors and importance of better stratifying IBD patients at risk of NAFLD and advanced liver fibrosis.

Objective: Chronic inflammatory disease increase arterial stiffness and are associated with accelerated atherosclerosis. Our aim was to determine augmentation index (AIx) and pulse wave velocity (PWV) in patients with chronic autoimmune liver disease. Design and method: We have enrolled 38 patients (3m 35w; age 58.7 ± 9.6) with chronic autoimmune liver disease (autoimmune hepatitis 4, primary biliary cholangitis 24, primary sclerosing cholangitis 10). Office blood pressure (BP) was using Omron M6; PWV and AIx by Arteriograph. The assessment of liver cirrhosis was determined with FibroScan. Fasting blood and 24-hour urine samples were collected. Hypertension was diagnosed in 42.1% patients (18.7% were treated) and diabetes in 8.4%. Results: PWV was 9.7 m/s while AIx was also increased (32.8%). PWV was positively correlated with age, sedimentation rate, CRP and central systolic BP and negatively with eGFR. AIx was positively correlated with heart rate and central systolic BP. Linear regression analysis showed positive association of Aix with duration of disease, sedimentation rate, total cholesterol,triglycerides and FibroScan stiffness. PWV was positively associated with age, duration of disease, sedimentation rate, total cholesterol and triglycerides. We found that patients with PWV > 9 m/s were significantly older, had higer sedimentation rates, lower GFR, higher total cholesterol, LDL cholesterol, systolic/diastolic BPr and central systolic BP values. Conclusions: Patients with chronic autoimmune liver diseases have increased arterial stiffness than general population which confirmed our hypothesis on impact of chronic inflammation on increased arterial stiffness. However, this should be confirmed on larger number of patients.